Axl receptor tyrosine kinase , together with Tyro3 and Mer , constitute the TAM family of receptor tyrosine kinases. In the nervous system , Axl and its ligand Growth-arrest-specific protein 6 (Gas6) are expressed on multiple cell types. Axl functions in dampening the immune response , regulating cytokine secretion , clearing apoptotic cells and debris , and maintaining cell survival. Axl is upregulated in various disease states , such as in the cuprizone toxicity-induced model of demyelination and in multiple sclerosis (MS) lesions , suggesting that it plays a role in disease pathogenesis. Axl expression correlates with poor prognosis in several cancers. Axl mediates multiple oncogenic phenotypes and activation of these RTKs constitutes a mechanism of chemoresistance in a variety of solid tumors. Axl contributes to cell survival , migration , invasion , metastasis and chemosensitivity justify further investigation of Axl as novel therapeutic targets in cancer. The receptor tyrosine kinase AXL is thought to play a role in metastasis. The soluble AXL receptor as a therapeutic candidate agent for treatment of metastatic ovarian cancer. GAS6/AXL targeting as an effective strategy for inhibition of metastatic tumor progression in vivo.
Axl receptor tyrosine kinase, together with Tyro3 and Mer, constitute the TAM family of receptor tyrosine kinases. In the nervous system, Axl and its ligand Growth-arrest-specific protein 6 (Gas6) are expressed on multiple cell types. Axl functions in dampening the immune response, regulating cytokine secretion, clearing apoptotic cells and debris, and maintaining cell survival. Axl is upregulated in various disease states, such as in the cuprizone toxicity-induced model of demyelination and in multiple sclerosis (MS) lesions, suggesting that it plays a role in disease pathogenesis. Axl expression correlates with poor prognosis in several cancers. Axl mediates multiple oncogenic phenotypes and activation of these RTKs constitutes a mechanism of chemoresistance in a variety of solid tumors. Axl contributes to cell survival, migration, invasion, metastasis and chemosensitivity justify further investigation of Axl as novel therapeutic targets in cancer. The receptor tyrosine kinase AXL is thought to play a role in metastasis. The soluble AXL receptor as a therapeutic candidate agent for treatment of metastatic ovarian cancer. GAS6/AXL targeting as an effective strategy for inhibition of metastatic tumor progression in vivo.
Zinc-α-2-Glycoprotein (AZGP1) can be found in blood plasma, seminal plasma, urine, sweat, saliva, liver, and epithelial cells of various human glands. AZGP1 has been proposed in the regulation of body weight, and the melanin production by normal and malignant melanocytes. AZGP1 stimulates lipid degradation in adipocytes and causes the extensive fat losses associated with some advanced cancers. AZGP1 has been reported to stimulate lipid breakdown and may have an important role in lipid homeostasis. Mature human AZGP1 consists of one MHC class I antigen region and a C2-type Ig-like domain. AZGP1 has two alternate splice forms, one shows a 66 amino acids substitution for the C-terminal 30 amino acids, the other one shows a nine Lys substitution for amino acid 151-298.
Azurocidin is an Azurophil granule antibiotic protein, with monocyte chemotactic and antibacterial activity. The Azurophil granules, specialized lysosomes of the neutrophil, contain at least 10 proteins implicated in the killing of microorganisms. Azurocidin is a member of the serine protease family that includes Cathepsin G, Neutrophil Elastase (NE), and Proteinase 3 (PR3), however, Azurocidin is not a serine proteinase since the active site serine and histidine residues are replaced. Human Azurocidin together with NE and PR3 are expressed coordinately and are packaged together into azurophil granules during neutrophil differentiation. Azurocidin has been identified as a modulator of endothelial permeability and an important multifunctional inflammatory mediator. Neutrophils arriving first at sites of inflammation release Azurocidin which acts in a paracrine fashion on endothelial cells causing the development of intercellular gaps and allowing leukocyte extravasation. Azurocidin thus be regarded as a reasonable therapeutic target for a variety of inflammatory disease conditions.
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